CYTOGENETICALLY NORMAL ACUTE MYELOID LEUKEMIA

Abstract

In recent years, a number of somatically acquired mutational changes have been identified in patients with acute myeloid leukemia (AML). Most of these genetic changes occur in normal-karyotype AML, representing the largest cytogenetic subgroup (40–50%) of AML. These molecular data not only provide new insight into the pathogenesis of AML, but also have clinical implications. In this review, we will discuss the most important gene changes, including mutations in the TP53 gene and mutations in the tyrosine kinase domain (TKD) of the FLT3 gene. These gene mutations have become important prognostic markers and now allow us to separate cytogenetically normal (CN)-AML into distinct prognostic subgroups. In addition, these mutant molecules are potential targets for molecular therapy.